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Atrial Natriuretic Peptide, Cyclic GMP Analogues and Modulation of Guanylyl Cyclase do not Alter Stimulated POMC Peptide Release From Perifused Rat or Sheep Corticotrophs
Author(s) -
Bowman Maria E.,
Robinson Phillip J.,
Smith Roger
Publication year - 1997
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1997.00665.x
Subject(s) - medicine , endocrinology , vasopressin , proopiomelanocortin , anterior pituitary , atrial natriuretic peptide , peptide hormone , corticotropic cell , chemistry , corticotropin releasing hormone , nitric oxide , neuropeptide , pituitary gland , arginine , soluble guanylyl cyclase , receptor , hypothalamus , hormone , biology , amino acid , cyclic gmp , biochemistry
Corticotrophin‐releasing hormone (CRH) and arginine vasopressin (AVP) are two potent stimulators for secretion of proopiomelanocortin (POMC)‐derived hormones, from corticotrophs. CRH also stimulates POMC synthesis. Atrial natriuretic peptide (ANP) has been reported to inhibit POMC peptide release and is thought to act through cGMP signalling pathways. A multicolumn cell perifusion system was used to investigate the role of cGMP signalling pathways in CRH‐ and AVP‐stimulated POMC peptide release from primary cultures of ovine or rat anterior pituitary cells. The CRH and/or AVP stimulations were applied at 30 min intervals as 5 min pulses, and the various treatments were infused over a period of 50 min, overlapping with 2 of the stimulations. ANP (10 nM) had no effect on β ‐endorphin ( β EP) release from ovine cells, stimulated by 0.5 nM CRH and 5 nM AVP together, or 5 nM CRH and 50 nM AVP separately. Rat anterior pituitary cells were stimulated with 0.05 nM CRH/0.5 nM AVP or 0.5 nM CRH/5 nM AVP and treated with 1 nM or 10 nM ANP, respectively. No inhibition of ACTH or β EP was observed. Similarly, the nitric oxide donors molsidomine (100 μM), SIN‐1 (100 μM) and NaNO 2 (100 μM) did not inhibit β EP release stimulated by 0.5 nM CRH/5 nM AVP in ovine cells. The cGMP analogues 8‐bromo‐cGMP (10 μM and 100 μM) and dibutyryl cGMP (100 μM) also had no effect on β EP and ACTH release from ovine or rat anterior pituitary cells. Dexamethasone (8 μM), a synthetic glucocorticoid known to block POMC synthesis and secretion of β EP and ACTH by a distinct mechanism, was used as a control and suppressed CRH/AVP‐stimulated β EP secretion from ovine anterior pituitary cells. These results contrast with some previous studies and demonstrate that the cGMP signalling pathway in sheep or rat anterior pituitary cells does not directly inhibit secretion of POMC‐derived hormones from corticotrophs.